reported the polyubiquitylation of multiple Lys residue of tau‐AC in the human AD brain.[5d] Because polyubiquitin chains can stabilize β‐strand stacking, we postulated that tau‐AC ubiquitylation, unlike phosphorylation, will further facilitate polymeric tau‐AC formation.[3] However, the mechanistic link between tau cleavage and its effect on PTM events (or vice versa) during the course of tauopathies remains to be determined. This evidence concerns the gene ASAH1 and Alzheimer disease.